Results 171 to 180 of about 1,831,838 (319)

Developmental programmes drive cellular plasticity, disease progression and therapy resistance in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
This study shows that lung adenocarcinomas exploit developmental branching morphogenesis to acquire a therapy resistant basal‐like tumour cell state. This process was found to be regulated by combined TP53 loss‐of‐function and type‐I interferon signalling, identifying a novel axis for biomarker and therapeutic target discovery.
Kamila J Bienkowska   +13 more
wiley   +1 more source

Stimulator of interferon genes agonist augmented antitumor immunity of osimertinib in Egfr‐mutated lung cancer

open access: yesMolecular Oncology, EarlyView.
Combining osimertinib with the STING agonist ADU‐S100 activates innate and adaptive immunity to overcome the non‐inflamed microenvironment of Egfr‐mutant lung cancer. This combination increases NK and CD8+ T‐cell infiltration, associated with activation of the STING‐IRF3 pathway and local immunogenic cell death.
Jun Nishimura   +19 more
wiley   +1 more source

Application of a new high performance liquid chromatography method to the pharmacokinetics of dibudipine in rats [PDF]

open access: yes
Purpose: To develop a HPLC method for assay of dibudipine in biological fluids and to study its pharmacokinetics in the rat. Methods. HPLC: 2 μl (20 μg/ml) mebudipine as internal standard, 0.2 ml NaOH 1 M and 2 ml ethyl acetate were added to 0.2 ml of ...
محمودیان, مسعود   +3 more
core  

Stable neuronal representations underlie cognitive resilience to Alzheimer's disease pathology. [PDF]

open access: yesAlzheimers Dement
Chen K   +9 more
europepmc   +1 more source

Rat Surveys and Rat Proofing

open access: yesAmerican Journal of Public Health and the Nations Health, 1937
openaire   +3 more sources

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

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